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Published on: April 25, 2025
How Tubular Epithelial Cell Injury Contributes to Renal Fibrosis
Bi-Cheng Liu1, Tao-Tao Tang2, Lin-Li Lv2
1Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing, China. liubc64@163.com.
Abstract:
The renal tubules are the major component of the kidney and are vulnerable to a variety of injuries including ischemia, proteinuria, toxins, and metabolic disorders. It has long been believed that tubules are the victim of injury. In this review, we shift this concept to renal tubules as a driving force in the progression of kidney disease. In response to injury, tubular epithelial cells (TECs) can synthesize and secrete varieties of bioactive molecules that drive interstitial inflammation and fibrosis. Innate immune-sensing receptors on the TECs also aggravate immune responses. Necroinflammation, an auto-amplification loop between tubular cell death and interstitial inflammation, leads to the exacerbation of renal injury. Furthermore, TECs also play an active role in progressive renal injury via mechanisms associated with the conversion into collagen-producing fibroblast phenotype, cell cycle arrest at both G1/S and G2/M checkpoints, and metabolic disorder. Thus, a better understanding the mechanisms by which tubular injury drives AKI and CKD is necessary for the development of therapeutics to halt the progression of CKD.
Insights
Renal tubules, often seen as victims of kidney injury, actively drive disease progression. Tubular epithelial cells (TECs) promote inflammation and fibrosis, worsening acute kidney injury (AKI) and chronic kidney disease (CKD).
Area of Science:
- Nephrology
- Cell Biology
- Immunology
Background:
- Renal tubules are crucial kidney components susceptible to various injuries.
- Traditionally viewed as passive victims, renal tubules are now recognized for their active role in kidney disease progression.
Purpose of the Study:
- To reframe the understanding of renal tubules from passive victims to active drivers of kidney disease.
- To explore the mechanisms by which tubular epithelial cells (TECs) contribute to interstitial inflammation, fibrosis, and overall renal injury.
Main Methods:
- Review of existing literature on renal tubule injury and kidney disease.
- Analysis of the molecular and cellular mechanisms involved in TEC responses to injury.
- Examination of the role of innate immune sensing and necroinflammation in exacerbating renal damage.
Main Results:
- Tubular epithelial cells (TECs) secrete bioactive molecules that promote interstitial inflammation and fibrosis.
- Innate immune-sensing receptors on TECs amplify immune responses.
- Necroinflammation creates a self-amplifying loop of cell death and inflammation, worsening kidney injury.
- TECs contribute to progressive renal injury through transdifferentiation into fibroblasts, cell cycle arrest, and metabolic dysregulation.
Conclusions:
- Renal tubules are active participants in the pathogenesis of acute kidney injury (AKI) and chronic kidney disease (CKD).
- Understanding TEC-driven mechanisms is crucial for developing novel therapeutics to halt kidney disease progression.
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